scholarly journals Acquired Complete Heart Block with Long QT Interval and Recurrent Polymorphic Ventricular Tachycardia: A Case Report

2016 ◽  
Vol 06 (02) ◽  
pp. 37-42
Author(s):  
Hosam Zaky ◽  
Jassem Al Hashmi
Keyword(s):  
Ventricular Tachycardia ◽  
Case Report ◽  
Qt Interval ◽  
Heart Block ◽  
Complete Heart Block ◽  
Polymorphic Ventricular Tachycardia ◽  
Long Qt ◽  
Long Qt Interval

Polymorphic ventricular tachycardia, ischaemic ventricular fibrillation, and torsade de pointes: importance of the QT and the coupling interval in the differential diagnosis

2021 ◽  
Author(s):  
Raphael Rosso ◽  
Aviram Hochstadt ◽  
Dana Viskin ◽  
Ehud Chorin ◽  
Arie Lorin Schwartz ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Ventricular Fibrillation ◽  
Qt Interval ◽  
Torsade De Pointes ◽  
Polymorphic Ventricular Tachycardia ◽  
Ectopic Beat ◽  
Long Qt ◽  
Drug Induced ◽  
Long Qt Interval ◽  
Coupling Interval

Abstract Aims Distinctive types of polymorphic ventricular tachycardia (VT) respond differently to different forms of therapy. We therefore performed the present study to define the electrocardiographic characteristics of different forms of polymorphic VT. Methods and results We studied 190 patients for whom the onset of 305 polymorphic VT events was available. The study group included 87 patients with coronary artery disease who had spontaneous polymorphic VT triggered by short-coupled extrasystoles in the absence of myocardial ischaemia. This group included 32 patients who had a long QT interval but nevertheless had their polymorphic VT triggered by ectopic beats with short coupling interval, a subcategory termed ‘pseudo-torsade de pointes] (TdP). For comparison, we included 50 patients who had ventricular fibrillation (VF) during acute myocardial infarction (‘ischaemic VF’ group) and 53 patients with drug-induced TdP (‘true TdP’ group). The QT of patients with pseudo-TdP was (by definition) longer than that of patients with polymorphic VT and normal QT (QTc 491.4 ± 25.2 ms vs. 447.3 ± 55.6 ms, P < 0.001). However, their QT was significantly shorter than that of patients with true TdP (QTc 564.6 ± 75.6 ms, P < 0.001). Importantly, the coupling interval of the ectopic beat triggering the arrhythmia was just as short during pseudo-TdP as during polymorphic VT with normal QT (359.1 ± 38.1 ms vs. 356.6 ± 39.4 ms, P = 0.467) but was much shorter than during true TdP (581.2 ± 95.3 ms, P < 0.001). Conclusions The coupling interval helps discriminate between polymorphic VT that occurs despite a long QT interval (pseudo-TdP) and polymorphic arrhythmias striking because of a long QT (true TdP).

scholarly journals Long QT interval induced by clindamycin: a case report

2018 ◽  
Vol 63 (1) ◽  
pp. 29 ◽  
Author(s):  
P B Maduranga ◽  
K C Chathurangani ◽  
C J Dharmaratne ◽  
U D De silva ◽  
S Amarasinghe
Keyword(s):  
Case Report ◽  
Qt Interval ◽  
Long Qt ◽  
Long Qt Interval

Medicolegal Problems in the Management of Cardiac Arrhythmias in Children

PEDIATRICS ◽  
1987 ◽  
Vol 79 (1) ◽  
pp. 84-88
Author(s):  
Arthur Garson
Keyword(s):  
Ventricular Tachycardia ◽  
Sudden Death ◽  
Cardiac Arrhythmias ◽  
Qt Interval ◽  
Long Qt ◽  
Seizure Disorders ◽  
Long Qt Interval ◽  
Potential Problems ◽  
Optimal Medical Management ◽  
Medicolegal Problems

Malpractice actions against pediatricians treating patients with arrhythmias have been recurrent in four general areas. Optimal medical management may not be widely recognized. Cases illustrating the following concepts are presented. (1) Intravenous verapamil therapy in babies may cause apnea, hypotension, and bradycardia; (2) continued episodes of atrial flutter in a child may cause sudden death; quinidine may be related to the death; (3) children with "familial seizure disorders" may in fact have the long QT interval syndrome. The QT interval must be measured on the ECG in patients with unexplained seizures; (4) "supraventricular tachycardia with aberration" is uncommon in children. Rapid heart rates with QRS complexes that are different from the sinus complexes are likely to be ventricular tachycardia. These situations must be recognized as potential problems and must be treated appropriately.

scholarly journals Tetrodotoxin-sensitive Navs contribute to early and delayed afterdepolarizations in long QT arrhythmia models

2018 ◽  
Vol 150 (7) ◽  
pp. 991-1002 ◽  
Author(s):  
Megan Koleske ◽  
Ingrid Bonilla ◽  
Justin Thomas ◽  
Naveed Zaman ◽  
Stephen Baine ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Action Potential ◽  
Qt Interval ◽  
Torsades De Pointes ◽  
Cellular Level ◽  
Polymorphic Ventricular Tachycardia ◽  
Wild Type ◽  
Long Qt ◽  
Delayed Afterdepolarizations

Recent evidence suggests that neuronal Na+ channels (nNavs) contribute to catecholamine-promoted delayed afterdepolarizations (DADs) and catecholaminergic polymorphic ventricular tachycardia (CPVT). The newly identified overlap between CPVT and long QT (LQT) phenotypes has stoked interest in the cross-talk between aberrant Na+ and Ca2+ handling and its contribution to early afterdepolarizations (EADs) and DADs. Here, we used Ca2+ imaging and electrophysiology to investigate the role of Na+ and Ca2+ handling in DADs and EADs in wild-type and cardiac calsequestrin (CASQ2)-null mice. In experiments, repolarization was impaired using 4-aminopyridine (4AP), whereas the L-type Ca2+ and late Na+ currents were augmented using Bay K 8644 (BayK) and anemone toxin II (ATX-II), respectively. The combination of 4AP and isoproterenol prolonged action potential duration (APD) and promoted aberrant Ca2+ release, EADs, and DADs in wild-type cardiomyocytes. Similarly, BayK in the absence of isoproterenol induced the same effects in CASQ2-null cardiomyocytes. In vivo, it prolonged the QT interval and, upon catecholamine challenge, precipitated wide QRS polymorphic ventricular tachycardia that resembled human torsades de pointes. Treatment with ATX-II produced similar effects at both the cellular level and in vivo. Importantly, nNav inhibition with riluzole or 4,9-anhydro-tetrodotoxin reduced the incidence of ATX-II–, BayK-, or 4AP-induced EADs, DADs, aberrant Ca2+ release, and VT despite only modestly mitigating APD prolongation. These data reveal the contribution of nNaVs to triggered arrhythmias in murine models of LQT and CPVT-LQT overlap phenotypes. We also demonstrate the antiarrhythmic impact of nNaV inhibition, independent of action potential and QT interval duration, and provide a basis for a mechanistically driven antiarrhythmic strategy.

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